Evidence map›Paper›PMID 9410894›Full record

ArticleThe Journal of clinical investigation1997

Genomic instability in the type II TGF-beta1 receptor gene in atherosclerotic and restenotic vascular cells.

T A McCaffrey, B Du, S Consigli, P Szabo, P J Bray, L Hartner, B B Weksler, T A Sanborn, G Bergman, H L Bush

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
5.8field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 168 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Molecular studies on coronary artery disease-a review.Indian journal of clinical biochemistry : IJCB · 2013
    Review
  8. Review
  9. Review
  10. Review
  11. Role of somatic mutations in vascular disease formation.Expert review of molecular diagnostics · 2010
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. The good smooth muscle cells in atherosclerosis.Current atherosclerosis reports · 2000
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 2 countries.

T A McCaffreyDepartment of Medicine, Cornell University Medical College-The New York Hospital, New York 10021, USA. tamccaf@med.cornell.edu
B Du
S Consigli
P Szabo
P J Bray
L Hartner
B B Weksler
T A Sanborn
G Bergman
H L Bush
Cornell University · USBritish Geriatrics Society · GB

Funding

SCOR IN MOLECULAR MEDICINE AND ATHEROSCLEROSISP50HL056987 · NHLBI · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI CRYSTAL, RONALD G · 1997 to 2001
$2.4M
TGF-B1 RECEPTORS IN RESTENOSIS AND AGINGR01AG012712 · NIA · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI MCCAFFREY, TIMOTHY A. · 1996 to 2000
$403k
NHLBI NIH HHS HL56987NIA NIH HHS R01 AG12712
6 · The paper itself

Abstract

Cells proliferating from human atherosclerotic lesions are resistant to the antiproliferative effect of TGF-beta1, a key factor in wound repair. DNA from human atherosclerotic and restenotic lesions was used to test the hypothesis that microsatellite instability leads to specific loss of the Type II receptor for TGF-beta1 (TbetaR-II), causing acquired resistance to TGF-beta1. High fidelity PCR and restriction analysis was adapted to analyze deletions in an A10 microsatellite within TbetaR-II. DNA from lesions, and cells grown from lesions, showed acquired 1 and 2 bp deletions in TbetaR-II, while microsatellites in the hMSH3 and hMSH6 genes, and hypermutable regions of p53 were unaffected. Sequencing confirmed that these deletions occurred principally in the replication error-prone A10 microsatellite region, though nonmicrosatellite mutations were observed. The mutations could be identified within specific patches of the lesion, while the surrounding tissue, or unaffected arteries, exhibited the wild-type genotype. This microsatellite deletion causes frameshift loss of receptor function, and thus, resistance to the antiproliferative and apoptotic effects of TGF-beta1. We propose that microsatellite instability in TbetaR-II disables growth inhibitory pathways, allowing monoclonal selection of a disease-prone cell type within some vascular lesions.

Indexed as

ArteriosclerosisAtherectomyBase SequenceCells, CulturedCoronary VesselsHumansMammary ArteriesMicrosatellite RepeatsMutationProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IIRisk FactorsProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type II

Identifiers

PMID9410894
PMCPMC508412
OpenAlexW2044063704

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.